An update on cancer stem cell survival pathways involved in chemoresistance in triple-negative breast cancer

Feb 12, 2025Future oncology (London, England)

Cancer stem cell survival pathways linked to chemotherapy resistance in triple-negative breast cancer

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Abstract

Triple-negative breast cancer (TNBC) relies on breast cancer stem cells (BCSCs) that exhibit significant treatment resistance.

BCSCs are associated with aggressive tumor behavior, metastasis, and recurrence in TNBC.
These cells possess self-renewal abilities and are resistant to conventional therapies.
Key signaling pathways such as Wnt, Hedgehog, and Notch are exploited by BCSCs for survival.
Mechanisms like drug efflux and enhanced DNA repair contribute to poor prognosis in TNBC patients.
The tumor microenvironment interacts with BCSCs, aiding their survival through stromal and immune cell interactions.
Emerging therapies targeting BCSCs, including immunotherapy and gene-editing, may disrupt these resistant cells.

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Triple-negative breast cancer (TNBC) presents a formidable global health challenge, marked by its aggressive behavior and significant treatment resistance. This subtype, devoid of estrogen, progesterone, and HER2 receptors, largely relies on breast cancer stem cells (BCSCs) for its progression, metastasis, and recurrence. BCSCs, characterized by their self-renewal capacity and resistance to conventional therapies, exploit key surface markers and critical signaling pathways like Wnt, Hedgehog, Notch, TGF-β, PI3K/AKT/mTOR and Hippo-YAP/TAZ to thrive. Their adaptability is underscored by mechanisms including drug efflux and enhanced DNA repair, contributing to poor prognosis and high recurrence rates. The tumor microenvironment (TME) further facilitates BCSC survival through complex interactions with stromal and immune cells. Emerging therapeutic strategies targeting BCSCs - ranging from immunotherapy and nanoparticle-based drug delivery systems to gene-editing technologies - aim to disrupt these resistant cells. Additionally, innovative approaches focusing on exosome-mediated signaling and metabolic reprogramming show promise in overcoming chemoresistance. By elucidating the distinct characteristics of BCSCs and their role in TNBC, researchers are paving the way for novel treatments that may effectively eradicate these resilient cells, mitigate metastasis, and ultimately improve patient outcomes. This review highlights the urgent need for targeted strategies that address the unique biology of BCSCs in the pursuit of more effective therapeutic interventions for TNBC.

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